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Published on: October 2, 2015
ADRB2 Modulates Asbestos-Induced Pleural Mesothelioma Progression by Influencing IL-17/NF-κB-Related Inflammatory
Shaoyang Huang1, Dandan Gu2, Jintao He3
1Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Health Science Center, Dali University, Dali 671000, Yunnan, PR China; Key Laboratory of Clinical Biochemistry Testing in Universities of Yunnan Province, College of Basic Medical Sciences, Dali University, Health Science Center, Dali 671000, Yunnan, PR China; Department of Cell Biology, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, Shaanxi, PR China.
This study identifies Adrenergic Receptor Beta 2 (ADRB2) as a key diagnostic and mechanistic target in asbestos-induced pleural mesothelioma (PM). ADRB2 is implicated in malignant progression and inflammatory signaling pathways, offering new avenues for PM diagnosis and treatment.
Area of Science:
- Toxicology and Carcinogenesis
- Molecular Biology and Genomics
- Oncology
Background:
- Pleural mesothelioma (PM) is an aggressive asbestos-related cancer with limited early diagnostic tools and poor prognosis.
- Understanding the molecular mechanisms of asbestos-induced PM is crucial for developing effective diagnostic and therapeutic strategies.
Purpose of the Study:
- To investigate the molecular mechanisms of asbestos-induced PM using network toxicology and integrated multi-omics analyses.
- To identify potential diagnostic biomarkers and therapeutic targets for asbestos-related PM.
Main Methods:
- Integrated analysis of asbestos-related targets from CTD with GEO transcriptomic datasets.
- Applied differential expression analysis, WGCNA, PPI analysis, functional enrichment, machine learning, and SHAP interpretation.
- Utilized immune-infiltration, single-cell RNA-sequencing, molecular docking, and cell-based assays (LDH, proliferation, invasion) with asbestos exposure.
Main Results:
- Identified Adrenergic Receptor Beta 2 (ADRB2) and other genes (LMO3, GPD1L, EDNRB, RNASE1, PDK4, CAT, MAL) as having strong diagnostic potential.
- ADRB2 showed mechanistic relevance, associated with immune cells in the PM microenvironment and modulated by asbestos exposure.
- Low-to-subtoxic asbestos concentrations (2.5 μg/cm²) promoted proliferation, invasion, and ADRB2 upregulation, with crocidolite being most potent.
- ADRB2 knockdown attenuated crocidolite-induced IL-17/NF-κB signaling, reduced pro-inflammatory cytokines, and suppressed malignant cell phenotypes.
Conclusions:
- ADRB2 is a promising diagnostic and mechanistic target for asbestos-induced pleural mesothelioma.
- ADRB2 plays a role in crocidolite-induced malignant progression via IL-17/NF-κB inflammatory signaling.
- These findings provide insights into PM pathogenesis and suggest potential therapeutic strategies targeting ADRB2.
